The three mammalian isoforms of transforming growth factor-beta(TGF-beta1, beta2, beta3) are potent regulators of cell growth, differentiation, and extracellular matrix deposition. To study their role in skin differentiation, we investigated the expression of TGF-beta isoforms on cell growth and differentiation induction of the human keratinocyte cell line, HaCaT by elevating the Ca(2+) concentration. An ELISA and RT-PCR assay revealed secreted TGF-beta 1 protein and TGF-beta 1 mRNA were increased during calcium-induced differentiation. In contrast, major differences were seen for TGF-beta 2 and TGF-beta 3 mRNA which were decreased during differentiation, but TGF-beta 2 and TGF-beta3 protein were not evident on an ELISA. These results suggest different functions for each TGF-beta isoforms in epidermal differentiation, such that TGF-beta 1 is associated with the more differentiated state, and TGF-beta 2 and TGF-beta 3 may be associated the more proliferated state.
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http://dx.doi.org/10.3346/jkms.2004.19.6.853 | DOI Listing |
Arch Insect Biochem Physiol
January 2025
State Key Laboratory of Agricultural and Forestry Biosecurity, Education Ministry Key Laboratory of Integrated Management of Crop Diseases and Pests/State & Local Joint Engineering Research Center of Green Pesticide Invention and Application, Department of Entomology, College of Plant Protection, Nanjing Agricultural University, Nanjing, China.
The activin cascade is activated when a pair of extracellular ligand (Myoglianin, Myo; Activin β, Actβ; Dawdle, Daw) binds to two pairs of transforming growth factor β (TGF) serine-threonine receptor kinases, TGF-β type I (Baboon, Babo) and II receptors. However, the roles of activin way have not well been explored in non-Drosophilid insects. In the present paper, we compared the functions of Activin β (Actβ) ligand and receptor isoform BaboB in post-embryonic development in a defoliating ladybird Henosepilachna vigintioctopunctata.
View Article and Find Full Text PDFAntioxidants (Basel)
November 2024
Department of Internal Medicine, Division of Cardiovascular Medicine, University of Michigan, Ann Arbor, MI 48109, USA.
Hypertension (HTN) is a major contributor to kidney damage, leading to conditions such as nephrosclerosis and hypertensive nephropathy, significant causes of chronic kidney disease (CKD) and end-stage renal disease (ESRD). HTN is also a risk factor for stroke and coronary heart disease. Oxidative stress, inflammation, and activation of the renin-angiotensin-aldosterone system (RAAS) play critical roles in causing kidney injury in HTN.
View Article and Find Full Text PDFbioRxiv
December 2024
Department of Nephrology and Mineral Metabolism, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, Tlalpan, Mexico City, Mexico.
The With No lysine (WNK) kinases regulate processes such as cell volume and epithelial ion transport through the modulation of Cation Chloride Cotransporters such as the NaCl cotransporter, NCC, present in the distal convoluted tubule (DCT) of the kidney. Recently, the interaction of WNKs with Nuclear Receptor Binding Protein 1 (NRBP1) and Transforming Growth Factor β-Stimulated Clone 22 Domain (TSC22D) proteins was reported. Here we explored the effect of NRBP1 and TSC22Ds on WNK signaling in vitro and in the DCT.
View Article and Find Full Text PDFMatrix Biol
January 2025
Department of Anatomy and Cell Biology, Dentistry, Schulich School of Medicine and Dentistry, Western University, London, Ontario, N6A 3K7, Canada; Dentistry, Schulich School of Medicine and Dentistry, Western University, London, Ontario, N6A 3K7, Canada. Electronic address:
Release of growth factors in the tissue microenvironment is a critical process in the repair and regeneration of periodontal tissues, regulating fibroblast behavior and phenotype. As a result of the complex architecture of the periodontium, distinct fibroblast populations in the periodontal ligament and gingival connective tissue exist in close proximity. Growth factor therapies for periodontal regeneration have gained traction, but quantification of their effects on multiple different fibroblast populations that are required for repair has been poorly investigated.
View Article and Find Full Text PDFPLoS Comput Biol
January 2025
Department of Hematology, Rheumatology and Infectious Disease, Faculty of Life Sciences, Kumamoto University, Kumamoto, Japan.
Human T-cell leukemia virus type 1 (HTLV-1) causes adult T-cell leukemia (ATL) and HTLV-1-associated myelopathy (HAM) after a long latent period in a fraction of infected individuals. These HTLV-1-infected cells typically have phenotypes similar to that of CD4+T cells, but the cell status is not well understood. To extract the inherent information of HTLV-1-infected CD4+ cells, we integratively analyzed the ATAC-seq and RNA-seq data of the infected cells.
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